Diagrammatic approach to excitonic effects on nonlinear optical response

Optical responses of atomically thin 2D materials are greatly influenced by electron-hole interactions. It is by far established that exciton signatures can be well-identified in the optical absorption spectrum of quasi-2D materials. However, the same level of understanding of excitonic effects on nonlinear optical responses and the ability to compute them accurately is still much desired. Based on the functional integral formalisms and working in the velocity gauge, we introduce a convenient Feynman diagram approach for calculating nonlinear responses including excitonic effects. By dressing electron-photon interactions with electron-hole ladder diagrams, we derive an expression for second-order optical responses and provide a comprehensive description of excitonic effects. We apply our approach to a monolayer h-BN model and show qualitative changes in the second harmonic generation spectrum when comparing with results assuming independent particles. Our approach can be readily extended to higher order optical responses and is feasible for first-principles calculations

RNAMST: efficient and flexible approach for identifying RNA structural homologs

[[abstract]]RNA molecules fold into characteristic secondary structures for their diverse functional activities such as post-translational regulation of gene expression. Searching homologs of a pre-defined RNA structural motif, which may be a known functional element or a putative RNA structural motif, can provide useful information for deciphering RNA regulatory mechanisms. Since searching for the RNA structural homologs among the numerous RNA sequences is extremely time-consuming, this work develops a data preprocessing strategy to enhance the search efficiency and presents RNAMST, which is an efficient and flexible web server for rapidly identifying homologs of a pre-defined RNA structural motif among numerous RNA sequences. Intuitive user interface are provided on the web server to facilitate the predictive analysis. By comparing the proposed web server to other tools developed previously, RNAMST performs remarkably more efficiently and provides more effective and flexible functions. RNAMST is now available on the web at http://bioinfo.csie.ncu.edu.tw/~rnamst/

Tauopathy

Tauopathy is a category of neurodegenerative diseases that are caused or associated with pathological tau protein. Some of the diseases are relatively common, which include Alzheimer’s disease (AD) and various Parkinsonism (PD). Tau protein is a type of microtubule-associated protein (MAP), encoded by the gene MAPT (microtubule-associated protein tau). Normally, tau binds to microtubule, supporting the assembling and structure of cytoskeletons. However, in tauopathy, normal tau protein undergoes abnormal posttranslational modifications and detaches from microtubule; furthermore, they may aggregate forming paired helical filaments (PHF) or straight filaments (SF). Abundant PHF could be observed under microscope as fibrillary tangles. In this chapter, we will introduce the pathogenesis process of tauopathy with regard to the posttranslational modifications of the protein, the animal models, and the developing treatments against tauopathy from a clinical prospective

RNAMST: efficient and flexible approach for identifying RNA structural homologs

RNA molecules fold into characteristic secondary structures for their diverse functional activities such as post-translational regulation of gene expression. Searching homologs of a pre-defined RNA structural motif, which may be a known functional element or a putative RNA structural motif, can provide useful information for deciphering RNA regulatory mechanisms. Since searching for the RNA structural homologs among the numerous RNA sequences is extremely time-consuming, this work develops a data preprocessing strategy to enhance the search efficiency and presents RNAMST, which is an efficient and flexible web server for rapidly identifying homologs of a pre-defined RNA structural motif among numerous RNA sequences. Intuitive user interface are provided on the web server to facilitate the predictive analysis. By comparing the proposed web server to other tools developed previously, RNAMST performs remarkably more efficiently and provides more effective and flexible functions. RNAMST is now available on the web at

SOHSite: incorporating evolutionary information and physicochemical properties to identify protein S-sulfenylation sites

Distribution of KEGG pathway annotations for S-sulfenylated proteins. (DOCX 15 kb

Quantum correlation generation capability of experimental processes

Einstein-Podolsky-Rosen (EPR) steering and Bell nonlocality illustrate two different kinds of correlations predicted by quantum mechanics. They not only motivate the exploration of the foundation of quantum mechanics, but also serve as important resources for quantum-information processing in the presence of untrusted measurement apparatuses. Herein, we introduce a method for characterizing the creation of EPR steering and Bell nonlocality for dynamical processes in experiments. We show that the capability of an experimental process to create quantum correlations can be quantified and identified simply by preparing separable states as test inputs of the process and then performing local measurements on single qubits of the corresponding outputs. This finding enables the construction of objective benchmarks for the two-qubit controlled operations used to perform universal quantum computation. We demonstrate this utility by examining the experimental capability of creating quantum correlations with the controlled-phase operations on the IBM Quantum Experience and Amazon Braket Rigetti superconducting quantum computers. The results show that our method provides a useful diagnostic tool for evaluating the primitive operations of nonclassical correlation creation in noisy intermediate scale quantum devices.Comment: 5 figures, 3 appendice

Enhancement of brain-type creatine kinase activity ameliorates neuronal deficits in Huntington's disease

AbstractHuntington's disease (HD) is a hereditary neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene. Brain-type creatine kinase (CKB) is an enzyme involved in energy homeostasis via the phosphocreatine–creatine kinase system. Although downregulation of CKB was previously reported in brains of HD mouse models and patients, such regulation and its functional consequence in HD are not fully understood. In the present study, we demonstrated that levels of CKB found in both the soma and processes were markedly reduced in primary neurons and brains of HD mice. We show for the first time that mutant HTT (mHTT) suppressed the activity of the promoter of the CKB gene, which contributes to the lowered CKB expression in HD. Exogenous expression of wild-type CKB, but not a dominant negative CKB mutant, rescued the ATP depletion, aggregate formation, impaired proteasome activity, and shortened neurites induced by mHTT. These findings suggest that negative regulation of CKB by mHTT is a key event in the pathogenesis of HD and contributes to the neuronal dysfunction associated with HD. In addition, besides dietary supplementation with the CKB substrate, strategies aimed at increasing CKB expression might lead to the development of therapeutic treatments for HD